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In the past 30 years, the field of pain management has increasingly
incorporated technologies of neurostimulation as part of the treatment
algorithm for patients with intractable pain. These technologies
include peripheral nerve stimulation, spinal cord stimulation, deep
brain stimulation, sacral nerve stimulation, and trigeminal nerve
stimulation. More and more patients with complex pain conditions
who have failed more conservative management are finding some degree
of relief through the use of these devices.
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The inspiration for development of these technologies came from
the landmark “gate control theory” introduced
by Melzack and Wall in 1965.1 Although this model
fails to explain certain phenomena seen in painful conditions and
cannot account for all of the observed effects of neurostimulation,
the gate control theory remains the primary paradigm used to describe
how neurostimulation acts to modify pain transmission. The gate control
theory is based on the presence of cells in the dorsal horn of the
spinal cord that receive afferent signals from peripheral C fibers
conveying painful stimuli, as well as non-nociceptive sensory fibers.
Once pain signals reach these dorsal horn interneurons, a “gate” is
activated and painful impulses propagate along ascending fibers
to the brain, resulting in conscious awareness of pain. Wall and
Melzack proposed that the gate could be closed to the transmission
of painful impulses through the selective activation of non-nociceptive
fibers. Thus, the notion of using neurostimulatory devices to preferentially
activate non-nociceptive fibers as a means of diminishing pain was
born.
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The application of neurostimulation has been increasing since
C. Norman Shealy implanted the first spinal cord stimulator device
in 1967. The scope of conditions amenable to these technologies
has likewise expanded as they have become more widely used in varying
populations of patients around the world. Current indications for
the use of these devices include isolated peripheral nerve injuries,
failed back surgery syndrome, peripheral vascular disease with critical
limb ischemia, refractory angina pectoris, deafferentation syndromes,
spinal-cord-injury–related pain, interstitial cystitis,
and trigeminal neuralgia. Other applications are continuously being
evaluated, including the use of spinal cord stimulation as a means
to monitor evoked potentials during thoracoabdominal aneurysm repair.2
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Although the gate control theory seems to explain the primary
mechanism by which neurostimulation works, it cannot account for
some of the clinically observed effects of spinal cord stimulation.
Some researchers have proposed that spinal cord stimulation inhibits
transmission of painful impulses partly by inducing a differential
conduction block of afferent nociceptive fibers via antidromic stimulation.
That the effects of stimulation can outlast the duration of the
stimulation would seem, however, to indicate this is not the only
mechanism by which neurostimulation influences pain transmission.
A number of investigators have speculated that neurohumoral mechanisms
are also involved. Studies have been conducted to further elucidate
which mediators may contribute. Substances that have been purported
to be involved in the neuromodulatory effects of spinal cord stimulation
include endogenous opioids, gamma (γ)-aminobutyric
acid (GABA), adenosine, substance P, serotonin, calcitonin gene-related
peptide (CGRP), ...